通过抑制储存运行的进入来抑制微质细胞迁移
Wei Tang1, Jiawen Peng1, Lixuan Chen1
1Department of Occupational Health and Occupational Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, Guangdong, China; Department of Occupational & Environmental Health and the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an 710032, China.
暴露于会抑制微质的迁移,这是神经炎症的一个关键特征. 这是通过降低储存运行的入量 (SOCE) 和损害STIM1功能,影响大脑健康而发生的.
科学领域:
- 神经科学是一个神经科学.
- 环境毒理学环境毒理学
- 细胞生物学 细胞生物学
背景情况:
- (Pb) 是一种持久性环境污染物,与神经毒性和神经炎症有关.
- 微质激活是神经炎症的核心,迁移是一个关键的细胞功能.
- 对微细胞迁移的具体影响仍然在很大程度上未知.
研究的目的:
- 为了研究 (Pb) 暴露对微质迁移的影响.
- 阐明底层机制,重点关注信号通路.
主要方法:
- 使用了BV-2微质细胞系和初级微质细胞.
- 在Pb治疗后评估了微质激活标志物 (TNF-α,CD206).
- 测量储存运行的入量 (SOCE) 和CRAC电流.
- 分析了STIM1,STIM2和Orai1.1的蛋白质水平.
- 通过STIM1过度表达来研究救援效应.
主要成果:
- Pb治疗增加了微质激活标志物 (TNF-α,CD206).
- 显著抑制了微质的迁移能力.
- Pb暴露剂量取决于下调的SOCE和CRAC电流.
- 在STIM1,STIM2或Orai1蛋白水平上没有发现显著变化.
- STIM1或其CRAC激活域的过度表达部分恢复了的流入和迁移.
结论:
- (Pb) 抑制了微细胞的迁移.
- 这种抑制是通过下调储存运行的入量的调节 (SOCE) 来实现的.
- 对STIM1功能的损伤在Pb诱导的微质迁移抑制中起着至关重要的作用.
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